2013
DOI: 10.4049/jimmunol.1301927
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Cutting Edge: Type 1 Diabetes Occurs despite Robust Anergy among Endogenous Insulin-Specific CD4 T Cells in NOD Mice

Abstract: Insulin-specific CD4+ T cells are required for type 1 diabetes. How these cells are regulated and how tolerance breaks down are poorly understood because of a lack of reagents. Therefore, we used an enrichment method and tetramer reagents to track insulin-specific CD4+ T cells in diabetes-susceptible NOD and resistant B6 mice expressing I-Ag7. Insulin-specific cells were detected in both strains, but they only became activated, produced IFN-g, and infiltrated the pancreas in NOD mice. Unexpectedly, the majorit… Show more

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Cited by 43 publications
(82 citation statements)
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“…Insulin specific CD4 þ T cells in B6. g7 mice maintained a naïve phenotype and were not able to produce IFNg upon restimulation, indicating that they may normally be maintained through ignorance [58]. In contrast, chromogranin A specific CD4 þ T cells were found at a similar frequency and had upregulated CD44 expression in the PcLN of both NOD and B6.…”
Section: Phenotyping Islet-specific T Cells In Nod Mice Reveals Multimentioning
confidence: 56%
See 3 more Smart Citations
“…Insulin specific CD4 þ T cells in B6. g7 mice maintained a naïve phenotype and were not able to produce IFNg upon restimulation, indicating that they may normally be maintained through ignorance [58]. In contrast, chromogranin A specific CD4 þ T cells were found at a similar frequency and had upregulated CD44 expression in the PcLN of both NOD and B6.…”
Section: Phenotyping Islet-specific T Cells In Nod Mice Reveals Multimentioning
confidence: 56%
“…Populations of CD4 þ T cells specific for both insulin and chromogranin A were detected in adult B6. g7 mice [58,60]. However, in protected B6.…”
Section: Phenotyping Islet-specific T Cells In Nod Mice Reveals Multimentioning
confidence: 94%
See 2 more Smart Citations
“…Hyperglycemic remission was ablated by administration of an anti-PD-L1 mAb, but Treg involvement in this setting was PD-L1-independent, indicating Treg alone did not mediate diabetes protection in this setting. Although, NOD mice have been shown to harbor anergic T cells which recognise InsB10-23, suggesting anergy may be broken in certain circumstances (Pauken et al, 2013). Furthermore, splenocytes coupled with both InsB9-23 and InsB15-23 significantly reduced diabetes incidence compared to sham-coupled splenocytes when injected into 4-5 week old NOD mice (Prasad et al, 2012).…”
Section: Discussionmentioning
confidence: 99%